Flashcards in neuroradiologyflash Deck (378):
Disk protrusion terminology
Bulge: Broad-based disk bulge. Usually bulging annulus fibrosus. Protrusion: Focal disk bulge. Usually herniated nucleus pulposus.
Intervertebral disk high intensity zone (HIZ)
High T2 signal of annulus indicating annular tear.
Disk free fragment mimickers
Conjoined root: Normal variant of two roots exiting thecal sac together. Same density of thecal sac. Tarlov cyst: Normal variant of dilated nerve root sleeve. Same density of thecal sac.
May cause nerve root impingement causing symptoms of a superior level. Nerve root has already exited central canal.
Common causes of Central Canal Stenosis
Facet joint degenerative change (most common). Lligamentum flavum hypertrophy.
Most common cause of neuroforaminal stenosis
Facet joint degenerative change with bony encroachment.
Lumbar spine bony canals where nerve roots lie after exiting thecal sac and before entering neuroforamen. Hypertrophy of superior articular facet is most common cause of encroachment.
Spondylolysis identified on axial images
Break in bony ring of the lamina (pars interarticularis) at the mid vertebral body level.
Spondylolisthesis occurs from either
Bilateral spondylolysis. Facet joint degenerative change.
Distinguishes postop scar from disk material
Scar tissue enhances. Disk material has only minimal peripheral enhancement.
Differentiates disk infection fromdegenerative disk disease at MR
Type 2 degenerative disk disease: Low T1 disk and high T2 parallel endplate bands. Disk space infection: High T2 disk.
Myelopathy neurologic signs
Ataxia. Bowel and bladder incontinence. Babinski sign.
Radiculopathy neurologic signs
Muscle weakness. Decreased reflexes. Dermatomal sensory deficits.
Urgency for imaging acute myelopathy
Poor prognosis if left untreated for greater than 24 hours.
Common causes of myelopathy
Extramedullary: Epidural mass cord compression. Cervical spine stenosis. Intramedullary: Tumor. Inflammation, Arteriovenous malformation (AVM). Spinal dural arteriovenous fistula (SPAVF).
Definition of Intramedullary spinal canal lesion
Usually confined to spinal cord. May be exophytic.
Definition of extramedullary spinal canal lesion
Outside of spinal cord. May be intradural or extradural.
Intradural intramedullary lesions
Ependymoma. Astrocytoma. Hemangioblastoma. Lipoma/(Epi)dermoid. Syringohydromyelia. Intramedullary AVM. Met/abscess (rare).
Intradural extramedullary lesions (includes subarachnoid space)
Meningioma. Schwannoma/neurinoma. Neurofibroma. Hemangiopericytoma. Lipoma/(Epi)dermoid. Arachnoid cyst/adhesion. Drop/leptomeningeal metastasis. Veins (extramedullary AVM).
Extradural extramedullary lesions
Degenerative: Herniated disc. Synovial cyst. Osteophyte. Rheumatoid pannus. Nondegenerative: Metastasis. Abscess. Hematoma. Primary tumor expansion or invasion. Epidural lipomatosis
Most common intramedullary lesion at MRI
Lupus Erythematosus spinal cord involvement
Areas of high T2 signal with cord swelling. May involve 4 or 5 vertebral segments. Have less well-defined margins than MS plaques.
Atlantoaxial instability and rheumatoid arthritis
Inflammatory changes (pannus) destroy transverse ligament of C1. Dens may slide posteriorly and intermittently compress cord causing myelomalacia. 5% of RA patients frank atlantoaxial instability.
Vertebral body and disc infection findings
Adjacent vertebral bodies and disc usually involved. Destruction greatest at endplates. Posterior elements usually spared. Low T1 and high T2 marrow signal with normal diffusion. If pyogenic disk enhances, granulation tissue extends above and below affected vertebrae.
Vertebral body neoplasm findings
Isolated or noncontiguous involvement. Pedicles typically affected. Low T1 and high T2 signal with restricted diffusion. Disk typically spared (except prostate cancer). Enhancement may obscure metastases within fatty marrow.
Vertebral body osteoporosis findings
Several vertebral bodies with height loss. Anterior weding with posterior elements spared. Normal T1 and T2 unless fracture. Disk spared.
TB of the spine, or Pott disease
Causes slow collapse of one or more vertebral bodies. Gibbus deformity, acute kyphosis. Infection spreads underneath longitudinal ligaments. Can lead to cord compression. May spare disks.
Most common neoplasm of the spine
Two most common primary intramedullary tumors
Spinal cord astrocytoma and ependymoma shared features
Expansile. Low T1 and high T2 signal with variable enhancement. Increased incidence in neurofibromatosis.
Spinal cord Ependymoma features
Most common spinal cord tumor in adults. Divided into cellular (intramedullary) and myxopapillary (filum terminale) types. Peak incidence inf ourth decade. Male predominance. These slow-growing neoplasms arise from ependymal cells lining the central canal of the cord or cell rests along the filum. Expansile. Low T1 and high T2 signal with variable enhancement. Increased incidence in neurofibromatosis.
Spinal cord Astrocytoma features
Most (75%) occur in cervical and upper to midthoracic cord. Fusiform cord widening. High T2 signal. Contrast enhancement over several vertebral body segments.
Occur in spinal cord and posterior fossa. High association with Von Hippel-Lindau syndrome. Densely enhancing nidus with related cyst and or cord expansion. May be extramedullary and multiple. May be mistaken for arteriovenous malformation (AVM).
Shorter term for syringohydromyelia. Hydromyelia, dilation of central canal and lined by ependyma. Syringomyelia, cavity outside central canal lined by glial cells. Suspect tumor as a cause of unexplained syrinx.
Most common intradural tumor in thoracic region
Spinal meningioma features
Most (80%) occur in women. Average age of 45. Multiple meningiomas suspicious for neurofibromatosis. Usually extramedullary/intradural. Can have extradural component. Dense calcification can occur. Dense homogenous enhancement. Broad dural tails.
Most common intraspinal mass
Spinal schwannoma features
Neuroforaminal extension and expansion are common in cervical and thoracic spine with intra and extraspinal components, dumbbell shape. In lumbar spine, tend to remain within dural sac.
Common intrathecal drop metastases
Subarachnoid seeding of primary CNS tumors: Posterior fossa medulloblastomas. Ependymomas. Pineal region neoplasms.
Most common spine extradural neoplasm
Metastatses: Breast, Lung, Prostate carcinoma.
Very low T1 and T2 marrow signal
Spinal AVM features
May be intramedullary or extramedullary. Intramedullary AVMs have a nidus of abnormal vessels that may cause hemorrhage or ischemia. Extramedullary AVMs generally are arteriovenous fistulas. Spinal dural arteriovenous fistulas (SDAVFs) cause symptoms through venous hypertension and congestion of the cord with edema.
Tethered Cord features
Low-lying conus medullaris. In a newborn conus normally at L2. Typically ascends one to two vertebral segments as child grows. May form a taut mass in posterior lumbar canal, obscuring conus/cauda junction.
Caudal Regression Syndrome
Hypoplastic or absent distal spine and sacrum. Blunted conus.
Spinal Arachnoid cysts and epidermoids
Similar to brain arachnoid cysts and epidermoids. Arachnoid cysts follow CSFsignal. Epidermoids restrict diffusion, bright on DWIs.
Spinal Epidural Hematoma
Ventral epidural space contains plexus of veins. These can tear in trauma, resulting in epidural hematoma.
Nerve Root Avulsion
Most commonly occur in cervical spine. Typically involve roots of brachial plexus and upper extremities. Birth trauma from shoulder traction is common example.
Acute versus chronic sinusitis findings
Acute sinusitis: Air-fluid levels and foamy secretions. Typically caused by viral URI. Chronic sinusitis: Mucoperiosteal thickening. Thickening of bony sinus walls.
Disease limited to the infundibulum of the maxillary ostium will result in
Isolated obstruction of maxillary sinus.
Lesion located at hiatus semilunaris (middle meatus) results in
Obstruction of ipsilateral maxillary sinus, anterior and middle ethmoid air cells, and frontal sinus. Described as ostiomeatal pattern of obstruction.
Sphenoid sinusitis is of great clinical concern as it may
Extend intracranially due to presence of valveless veins.
Sinus mucous retention cyst versus mucocele
Mucous retention cyst: Obstructed mucous glands within mucosal lining. Usually round. 1 to several cm in diameter. Mucocele: Entire sinus is obstructed. Expansion of sinus. Sinus wall bony thinning and remodeling. Mass may be present obstrucing draining ostium.
Neoplastic epithelium inverts and grows into underlying mucosa of lateral nasal wall. Surgically resected due to association with squamous cell carcinoma.
Juvenile nasopharyngeal angiofibromas
Male adolescents with epistaxis. Benign tumor but can be locally aggressive. Fills nasopharynx and bows posterior wall of maxillary sinus forward. Retromaxillary pterygopalatine fossa location is a hallmark feature. Avidly enhance.
Malignancies of paranasal sinuses and nasal cavity.
Squamous cell carcinoma. Lymphoma. Minor salivary tumors.
Most common salivary malignancies include
Adenoid cystic carcinoma. Adenocarcinoma. Mucoepidermoid carcinoma.
Arises from neurosensory receptor cells of olfactory nerve and mucosa. Occurs anywhere from cribriform plate to turbinates. Often quite destructive by time of diagnosis. Usually found high within nasal vault.
Three most common primary (mets by far more common) skull base malignant tumors
Chordoma (destructive midline mass). Chondrosarcoma. Osteogenic sarcoma (from radiation or Paget's degeneration).
Soft tissue mass (epidermoid cyst of desquamating stratified squamous epithelium) within middle ear cavity. Typically associated with bone erosion. Superior tympanic membrane (pars flaccida) is the most common site. CT images extent of disease.
Opacified petrous apex differential
Retained fluid secretions: Dark T1, bright T2, no enhancement. Petrous apicitis: Dark T1, bright T2, and ring enhancement. Nonaerated petrous apex: Bone marrow, bright T1, dark T2, and no enhancement. Cholesterol granuloma: Hemorrhagic component, bright T1 and T2.
Granulation tissue within partially obsructed petrous air cells. Have cholesterol and hemorrhagic component (high T1 and T2 signal).
Deep anatomy of the head and neck is subdivided by layers of deep cervical fascia into the following spaces:
(1) Superficial mucosal. (2) Parapharyngeal. (3) Carotid. (4) Parotid. (5) Masticator. (6) Retropharyngeal. (7) Prevertebral.
Mucosal head and neck compartment contents
Squamous mucosa. Lymphoid tissue (adenoids, lingual tonsils). Minor salivary glands.
Mucosal head and neck compartment pathology
Nasopharyngeal carcinoma. Squamous cell carcinoma. Lymphoma. Minor salivary gland tumors. Juvenile angiofibroma. Rhabdomyosarcoma.
Parapharyngeal head and neck compartment contents
Fat. Trigeminal nerve (V3). Internal maxillary artery. Ascending pharyngeal artery.
Parapharyngeal head and neck compartment pathology
Minor salivary gland tumor. Lipoma. Cellulitis/abscess. Schwannoma.
Parotid head and neck compartment contents
Parotid gland. Intraparotid lymph nodes. Facial nerve (VII). External carotid artery. Retromandibular vein.
Parotid head and neck compartment pathology
Salivary gland tumors. Metastatic adenopathy. Lymphoma. Parotid cysts.
Carotid head and neck compartment contents
Cranial nerves IX–XII. Sympathetic nerves. Jugular chain nodes. Carotid artery. Jugular vein.
Carotid head and neck compartment pathology
Schwannoma. Neurofibroma. Paraganglionoma. Metastatic adenopathy. Lymphoma. Cellulitis/abscess. Meningioma.
Masticator head and neck compartment contents
Muscles of mastication. Ramus and body of mandible. Inferior alveolar nerve.
Masticator head and neck compartment pathology
Odontogenic abscess. Osteomyelitis. Direct spread of squamous cell carcinoma. Lymphoma. Minor salivary tumor. Sarcoma of muscle or bone.
Retropharyngeal head and neck compartment contents
Lymph nodes (lateral and medial retropharyngeal). Fat.
Retropharyngeal head and neck compartment pathology
Metastatic adenopathy. Lymphoma.
Prevertebral head and neck compartment contents
Cervical vertebrae. Prevertebral muscles. Paraspinal muscles. Phrenic nerve.
Prevertebral head and neck compartment pathology
Osseous metastases. Chordoma. Osteomyelitis. Cellulitis. Abscess.
Benign midline nasopharynx lesion of high T2 signal. Believed to be remnant of notochordal tissue (benign).
Most common minor salivary gland malignancy and has propensity for perineural spread
Adenoid cystic carcinoma
The parapharyngeal space is surrounded by what spaces
the carotid space posteriorly, the parotid space laterally, the masticator space anteriorly, and the superficial mucosal space medially. Therefore, the parapharyngeal space will be compressed on its medial surface by masses originating from the mucosal surface, displaced anteriorly by carotid sheath masses, displaced medially by parotid masses, and displaced posteriorly and medially by masses within the masticator space.
Triad of nasopharyngeal malignancy
1) Mucosal mass of lateral nasopharynx (fossa of Rosenmuller). (2) Lateral retropharyngeal nodes. (3) Mastoid opacification (eustachian tube dysfunction)
Head and neck paragangliomas
Vascular tumors arising from neural crest cell derivatives. Names given according to location: Carotid body tumor (at carotid bifurcation). Glomus vagale tumor (vagus nerve). Glomus jugulare tumor (jugular ganglion of vagus nerve). Glomus tympanicum tumor (Arnold and Jacobson nerves of middle ear).
Salivary gland tumors
Benign: Pleomorphic adenoma. Warthin tumor. Malignant: Adenocystic carcinoma. Adenocarcinoma. SCC. Mucoepidermoid carcinoma.
Head and neck trans-spatial disease categories
Lymphatic masses (lymphangioma). Neural masses (neurofibroma, schwannoma, perineural spread of tumor). Vascular masses (hemangioma).
Head and neck diseases that demonstrate perineural spread
Fungal infections. Squamous cell carcinoma. Adenoid cystic carcinoma.
This lymph node chain serves as the final common afferent pathway for lymphatic drainage of the entire head and neck.
Internal jugular nodal chain
Pathologic size of head and neck lymph nodes
Jugulodigastric and submandibular nodes may normally measure up to 1.5 cm. All other nodes up to 1.0 cm.
Common optic nerve sheath complex tumors
Optic nerve glioma. Optic sheath meningioma.
Optic nerve glioma
Low grade pilocytic astrocytoma. Most common tumor of optic nerve. Typically occurs during first decade of life. High association with neurofibromatosis type 1. Enlarged sheath complex may be tubular, fusiform, or eccentric with kinking. Rarely calcify.
Arachnoidal hyperplasia or gliomatosis
Thickening of perioptic meninges associated with optic nerve gliomas. Reflects peritumoral reactive meningeal change.
Optic sheath meningiomas
Grow in a linear fashion along optic nerve. Tram track pattern of linear enhancement. May invade through dura. May be extensively calcified.
Orbital vascular lesions and age groups
Capillary hemangiomas, infants (younger than 1 year). Diagnosed within first weeks of life. Lymphangiomas, older group of children (3 to 15 years). Propensity to bleed. Often contain blood degradation products. Cavernous hemangiomas, adults. Sharply circumscribed and round. Venous varix, generally in adults. Dilated vein. Changes with Valsalva maneuver.
Superior ophthalmic vein pathology
Thrombosis often occurs with cavernous sinus thrombosis. Loss of normal flow void. Enlargement occurs with cavernous carotid fistulas.
Most common cause of intraorbital mass in an adult
Idiopathic inflammatory pseudotumor. Inflammatory lymphocytic infiltrate. Involves tendinous attachments to the globe. Often rapidly develops presenting with painful proptosis, chemosis, and ophthalmoplegia.Lymphoma tends to present with painless proptosis.
3 common adult intraorbital masses
Idiopathic inflammatory pseudotumor. Cavernous hemangioma. Lymphoma.
Enlargement of extraocular muscles with sparing of tendinous attachments to the globe
Thyroid ophthalmopathy (Graves disease). Causes unilateral or bilateral proptosis in adults. Muscles involved, in decreasing order: I'M SLow. Inferior rectus. Medial rectus. Superior rectus. Lateral retus.
Lesions of the lacrimal gland
Inflammatory: Sarcoidosis. Sjogren syndrome. Neoplastic: Salivary gland (mixed-cell tumor or adenoid cystic carcinoma). Lymphoma. Pseudotumor. Dermoid (fat-fluid level).
Most common primary ocular malignancy. Leukocoria. Calcified ocular mass.
Epithelium-lined tract along which primordial thyroid gland migrates. Extends from foramen cecum (tongue base) to anterior of thyrohyoid membrane and strap muscles to ends at thyroid isthmus. Normally involutes by 8 to 10 weeks of gestation. May give rise to cyst, sinus tract, or ectopic thyroid tissue.
The usual clinical presentation is that of a painless neck mass along the anterior border of the sternocleidomastoid muscle, presenting during the first to third decade.
Second branchial cleft cyst. Anterior to mid sternocleidomastoid muscle. Lateral to internal jugular vein at the level of carotid bifurcation.
Congenital malformations of lymphatic channels. Benign and nonencapsulated. Classified as capillary, cavernous, or cystic. Most present at birth or during infancy.
Soft tissue swelling of the scalp located beneath subcutaneous fibrofatty tissue and above temporalis muscle.
Intracranial air, pneumocephalus, may be seen with what fractures
Compound skull fractures. Fractures involving paranasal sinuses.
Epidural hematoma generalities
Usually arterial in origin. Often result from skull fracture disrupting middle meningeal artery.Strips dura from inner table of the skull. Forms an ovoid mass. Generally does not cross suture lines.
Venous epidural hematomas
Less common than arterial epidurals. Tend to occur at the vertex, posterior fossa, or anterior aspect of middle cranial fossa. Usually result from disrupted dural venous sinuses. Vertex epidurals can cross sagittal suture.
Typically result from tearing of cortical veins that traverse the subdural space. Will not cross falx cerebri or tentorium. Can cross sutural margins. Frequently layer along hemispheric convexity from anterior falx to posterior falx. Crescent-shaped in axial plane. Biconvex in coronal plane.
Result from disruption of small subarachnoid vessels, aneurysm, or direct extension by a contusion or hematoma. Hyperdense linear areas within cisterns and sulci. May lead to subsequent hydrocephalus by impaired CSF resorption at the arachnoid villi.
May result from tearing of subependymal veins, direct extension of parenchymal hematoma, retrograde flow of subarachnoid hemorrhage. Risk of hydrocephalus by obstruction of the aqueduct or arachnoid villi. Hyperdense material layering within ventricular system.
Diffuse axonal injury (DAI)
Widespread disruption of axons due to acceleration or deceleration injury. Small, petechial hemorrhages at gray-white junction of cerebral hemispheres and or corpus callosum.
T2 and DW bright and ADC dark.
Focal brain injury involving superficial gray matter. Occur near bony protuberances: Temporal lobes above petrous bone or posterior to greater sphenoid wing. Frontal lobes above cribriform plate, planum sphenoidale, and lesser sphenoid wing.
Traumatic Intracerebral Hematoma
Rupture of small intraparenchymal blood vessels. Tend to have less surrounding edema than cortical contusions. Most are located in the frontotemporal white matter.
Traumatic subcortical gray matter injury
Uncommon manifestation of primary intra-axial injury. Multiple petechial hemorrhages primarily affecting basal ganglia and thalamus.
Von Hippel-Lindau syndrome imaging manifestations
Visceral: Renal cell carcinomas. Pheochromocytomas. Pancreatic islet cell tumors. Pancreatic, hepatic, renal, and splenic cysts. CNS: Retinal capillary hemangiomas. Spinal cord and posterior fossa hemangioblastomas. Endolymphatic sac adenocarcinomas.
Distinguishing epidermoids from arachnoid cysts on MR imaging.
Both follow CSF T1 and T2 signal. Epidermoids restrict diffusion, are bright at DWI. Arachnoid cysts do not restrict diffusion. Epidermoids are composed of epithelial cells that grow in layers. Arachnoid cysts contains CSF.
Pachymeningeal versus leptomeningeal enhancement findings unfinished.
Pachymeningeal enhancement is characteristically thick, smooth, and uninterrupted.
Rare cystic lesion classically located at the anterior roof of the third ventricle at the foramen of Monro.
Colloid cyst. Generally are hyperdense to brain parenchyma. Do not enhance.
Carotid cavernous fistula (CCF)
Communication between cavernous portion of internal carotid artery and surrounding venous plexus. Typically follows a full-thickness arterial injury. Results in venous engorgement of cavernous sinus, ipsilateral superior ophthalmic vein, inferior petrosal sinus.
Diffuse cerebral edema CT imaging findings
Decreased cerebral density. Loss of gray-white differentiation. Usually spares cerebellum and brainstem, which appear relatively hyperdense.. Falx and cerebral vessels may appear dense, mimicking acute subarachnoid hemorrhage.
Most common form of brain herniation. Cingulate gyrus is displaced across midline under the falx. May compress adjacent lateral ventricle. May enlarge contralateral ventricle (obstruction of the foramen of Monro). Both anterior cerebral arteries may be displaced to contralateral side.
Medially displaced medial temporal lobe over free margin of tentorium. Focal effacement of ambient cistern and lateral suprasellar cistern. Rarely compresses contralateral cerebral peduncle (Kernohan's notch) against tentorial margin.
Descending transtentorial herniation: Effacement of suprasellar and perimesencephalic cisterns. Pineal calcification is displaced inferiorly. Ascending transtentorial herniation: May involve vermis and parts of cerebellar hemispheres. Large posterior fossa hematomas
Known as a growing fracture. Caused by traumatic tear of the dura. Outpouching of arachnoid at site of suture or skull fracture.
Midline hematoma within tegmentum of rostral pons and midbrai. Associated with descending transtentorial herniation. Due to stretching or tearing of penetrating arteries.
Nonaccidental trauma head findings
Skull fractures. Subdural hematomas. Diffuse brain swelling.
Moya moya disease
Rare leptomeningeal vascular collaterals that form due to stenosis or occlusion of Circle of Willis arteries. Puff of smoke appearance at angiography. Associations: Sickle cell disease. Neurofibromatosis type I. Down's syndrome. Fibromuscular dysplasia.
Differential diagnosis of supratentorial partially cystic, partially solid mass in a child:
Pilocytic astrocytoma. PNET (primitive neuroectodermal tumor). Hemorrhage.
Le Fort I
Floating palate. Horizontal fracture through maxillary sinuses, nasal septum, and inferior ptyergoid plates.
Le Fort II
Pyramidal fracture through bridge of nose, medial orbits, lateral and posterior maxillary walls, nasal septum, inferior orbital rim (infraorbital nerve injury), and midportion of ptyergoid plates.
Le Fort III
Craniofacial dysjunction. Horizontal fracture through orbits. Begins near nasofrontal suture and extends posteriorly through nasal septum, medial and lateral orbit walls, zygomatic arch, and base (superior aspect) of pterygoid plates.
CT scans done within 6 hours of MCA occlusion will commonly exhibit
Insular ribbon sign: Subtle blurring of gray-white layers of insula. Caused by early edema. Lentiform nucleus edema sign: Hypodense putamen.
ischemic but not infarcted (salvageable) tissue. Peri-infarct tissue.
Diffusion-Weighted MR in Acute Ischemia
Brain water diffusion rates fall rapidly during acute ischemia. Bright signal on DWIs.
Apparent diffusion coefficient (ADC).
Reflects pure diffusion behavior. Free of underlying T2 contributions (shine through or dark through).
Fluid-Attenuated Inversion Recovery (FLAIR) in Ischemia
Suppresses free water CSF signal but allows T2 weighting of parenchyma. Increases conspicuity of T2 changes in ischemia. May help detect small cortical lesions and acute subarachnoid hemorrhage.
CT finding occuring during 2nd week after infarction. Cerebral edema and mass effect subside while proteins accumulate from cell lysis. Injurred brain morphology and density appear normal at CT.
Hemorrhagic Transformation of Infarction
Seen 1 to 2 weeks postinfarction. Hemorrhage of reperfused capillaries. Serpiginous line of petechial blood following gyral contours of infarcted cortex.
Time course of CT-detected enhancement of infarcted brain
Begins at about 1 week. Peaks at 7 to 14 days. Often assumes a gyral pattern. As gliosis ensues and blood-brain barrier is repaired, enhancement fades and resolves by 3 months.
Intravascular MR enhancement of infarcted brain
Commonly seen in infarct during the first week. May be due to slow flow or vasodilation in arteries and veins. May be detected within minutes of vessel occlusion. Seen in a majority of cortical infarcts at 1 to 3 days. Resolves by 10 days.
Maximal brain swelling post brain infarction occurs at what days
3 to 7 days postinfarction.
Encephalomalacia post brain infarction occurs when
30 to 90 days (1 to 3 months) postinfarction.
ACA (anterior cerebral artery) three subgroups:
Medial lenticulostriate branches: Rostral portions of basal ganglia. Pericallosal branches: Corpus callosum. Hemispheric branches: Medial frontal and parietal lobes.
Two main branch groups of MCA (middle cerebral artery)
Lateral lenticulostriate branches: Supply most of basal ganglia. Hemispheric branches: Lateral cerebral surface.
Major branches of PCA (posterior cerebral artery)
Midbrain and thalamic perforating branches. Posterior choroidal arteries. Cortical branches to medial temporal and occipital lobes.
(Deficit/Syndrome : Cerebral artery/branch/side affected), Leg weakness :
ACA/Hemispheric branch/either side
(Deficit/Syndrome : Cerebral artery/branch/side affected), Incontinence, akinetic mutism :
ACA/Hemispheric branch/both sides
(Deficit/Syndrome : Cerebral artery/branch/side affected), Facial weakness :
ACA/Medial lenticulostriates/either side
(Deficit/Syndrome : Cerebral artery/branch/side affected), Dysarthria with or without motor aphasia :
(Deficit/Syndrome : Cerebral artery/branch/side affected), Face and arm weakness > leg weakness :
MCA/Hemispheric branch/either side
(Deficit/Syndrome : Cerebral artery/branch/side affected), Motor aphasia (anterior lesion) :
(Deficit/Syndrome : Cerebral artery/branch/side affected), Receptive aphasia (posterior lesion) :
(Deficit/Syndrome : Cerebral artery/branch/side affected), Global aphasia :
MCA/Hemispheric branch (total)/Left
(Deficit/Syndrome : Cerebral artery/branch/side affected), Neglect syndromes :
(Deficit/Syndrome : Cerebral artery/branch/side affected), Visulospatial dysfunction :
(Deficit/Syndrome : Cerebral artery/branch/side affected), Variable lacunar syndromes :
MCA/Lateral lenticulostriate branches/Either
(Deficit/Syndrome : Cerebral artery/branch/side affected), Hemianopsia :
(Deficit/Syndrome : Cerebral artery/branch/side affected), Cortical blindness :
(Deficit/Syndrome : Cerebral artery/branch/side affected), Memory deficits :
(Deficit/Syndrome : Cerebral artery/branch/side affected), Somnolence :
(Deficit/Syndrome : Cerebral artery/branch/side affected), Sensory disturbances :
(Deficit/Syndrome : Cerebral artery/branch/side affected), Ataxia, vertigo, vomiting :
Cerebellar/PICA, AICA, or SCA/ Either
(Deficit/Syndrome : Cerebral artery/branch/side affected), Coma if mass effect :
Cerebellar/PICA, AICA, or SCA/ Either
(Deficit/Syndrome : Cerebral artery/branch/side affected), ± brainstem deficits :
Cerebellar/PICA, AICA, or SCA/ Either
(Deficit/Syndrome : Cerebral artery/branch/side affected), Man-in-a-barrel syndrome :
(Deficit/Syndrome : Cerebral artery/branch/side affected), Severe memory problems :
Order of cerebellar branches going from top to bottom can be remembered using the acronym
SAP: Superior cerebellar artery. Anterior inferior cerebellar artery. Posterior inferior cerebellar artery.
Superior vermis. Middle and superior cerebellar peduncles. Superolateral aspects of cerebellar hemispheres.
Anterior Inferior Cerebellar Arteries (AICA) arise from
Proximal basilar artery.
Posterior Inferior Cerebellar Arteries (PICA) arise from
Distal vertebral artery, 1 to 2 cm below basilar origin.
Involvement of the medulla in PICA infarction adds elements of Wallenberg syndrome, which include
Ataxia. Facial numbness. Horner syndrome. Dysphagia. Dysarthria.
Small subcortical infarcts. May occur in any territory. Characteristic locations: Lenticular nucleus (37%). Pons (16%). Thalamus (14%). Caudate (10%). Internal capsule/corona radiata (10%).
Beginning at the genu and working back, the internal capsule carries somatotopically organized fibers
Corticobulbar fibers. HAL: Head fibers. Arm fibers. Leg fibers.
Virchow-Robin spaces. May simulate lacunes. Follow CSF signal. No mass effect. Occur along path of a penetrating vessel.
Small-Vessel Ischemic Changes
Small foci of T2 hyperintensity scattered throughout brains of older patients. May or may not have clinical symptoms. Commonly associated with patchy or diffuse T2 hyperintensity in the centrum semiovale.
Some cerebral vasculitides
Autoimmune disorders. Drug exposure (heroin, amphetamines). Polyarteritis nodosa. Idiopathic processes (giant cell arteritis).
Venous sinus thrombosis predisposing factors include
Hypercoagulable states. Pregnancy. Infection (spread from contiguous scalp, face, middle ear, or sinus). Dehydration. Meningitis. Direct invasion by tumor.
Empty delta sign
Filling defect within sagittal sinus on postcontrast CT. Indicates venous sinus thrombosis.
Superficial hemosiderosis (or superficial siderosis)
Diffuse hemosiderin deposition on brain surface. Due to large or recurrent subarachnoid hemorrhages.
MR oxyhemoglobin per time, RBC, and T1 and T2 signal
Less than 1 day. RBC intact. T1 iso/dark. T2 bright.
MR deoxyhemoglobin per time, RBC, and T1 and T2 signal
0-2 days. RBC intact. T1 iso/dark. T2 dark.
MR methemoglobin (intracellular) per time, RBC, and T1 and T2 signal
2-14 days. RBC intact. T1 bright. T2 dark.
MR methemoglobin (extracellular) per time, RBC, and T1 and T2 signal
10-21 days. RBC lysed. T1 bright. T2 bright.
MR hemosiderin/ferritin per time, RBC, and T1 and T2 signal
> 21 days. RBC lysed. T1 dark. T2 dark.
Most sensitive areas for detecting SAH
Dependent parts of occipital horns. Interpeduncular fossa.
Main finding in patients whose condition continues to deteriorate after the initial SAH
Infarcts from post SAH increased intracranial pressure or arterial vasospasm.
Congenital berry aneursym
May be due to congenital absence of arterial media. Those larger than 3 to 5 mm are at increased risk for rupture. Often occur near branch points of circle of Willis.
Distal branch cerebral aneurysms are seen in what conditions
Prior trauma. Systemic infection (bacterial endocarditis with mycotic aneurysm).
Besides berry aneursyms, list other causes of cerebral aneurysms
Atherosclerosis. Fibromuscular disease. Polycystic kidney disease. Mycotic. Post-traumatic.
Main differential considerations for cerebral parenchymal hemorrhage
Hypertensive hemorrhage. Vascular malformations. Drug effects. Amyloid angiopathy. Bloody tumors.
Common locations for intracranial hypertensive hemorrhages
Putamen (35% to 50%). Subcortical white matter (30%). Cerebellum (15%). Thalamus (10% to 15%). Pons (5% to 10%).
Intracranial hemorrhage cause in young patients, less common than hypertension
Vascular malformations: AVMs. Cavernous malformations. Telangiectasias. Venous malformations.
Most common type of brain vascular malformation. Abnormal tangle of arteries directly connected to veins without intervening capillaries. Most present with hemorrhage or seizures. 2% to 3% annual risk of bleeding,
Thin-walled sinusoidal vessels (neither arteries nor veins). May present with seizures or small parenchymal hemorrhages.
Anomalous veins that drain normal brain. Occur in 1% to 2% of patients. Enlarged enhancing stellate venous complex that extends to ventricular or cortical surface.
Amyloid angiopathy cerebral hemorrhage
Can cause intracranial, frequently lobar, hemorrhage. Amyloid deposits within media and adventitia of medium size and small cortical arteries. Not associated with systemic vascular amyloidosis. Affects elderly.
Hemorrhagic cerebral neoplasm
Primary: Glioblastomas. Metastatses: Bronchogenic carcinoma. Thyroid. Melanoma. Choriocarcinoma. Renal cell carcinoma.
Features of Benign Versus Malignant Intracranial Hemorrhage
Benign: Complete hemosiderin rim. Mild edema. Minimal acute enhancement (unless AVM). Blood products evolve from periphery to center. Malignant: Delayed or incomplete hemosiderin ring. Moderate surrounding edema. Moderate to severe acute enhancement. Irregular or complex blood product evolution.
Glial cell intracranial neoplasms (gliomas)
Astrocytoma. Oligodendroglioma. Ependymoma. Choroid plexus tumor.
Nerve sheath intracranial neoplasms
Tumors occuring along brain meninges or within the ventricles. Most nonglial tumors.
Significant general midline shift, if shift is greater than
Hallmarks of uncal herniation?
Effacement of ambient cistern. Contralateral hydrocephalus. May compromise ipsilateral oculomotor (III) nerve (pupillary dilation).
Differentiating a small neoplasm from a small infarct may be very difficult. When can followup imaging be obtained to help distinguish between the two.
Virtually all infarcts will be smaller in size by 3 weeks. If lesion is same size or larger at 3 weeks, a neoplasm should be favored.
Extra-axial mass refers to
Everything outside the brain: Arachnoid. Meninges. Dural sinuses. Skull. Ventricles.
White matter buckling?
Extra-axial lesions may buckle white matter. Inward compression of white matter (thinning of fronds). Preserved gray-white matter differentiation.
Tumors of high cellular density
Usually small cell tumors (high nucleus:cytoplasm ratio, hyperdense and T2 hypointense): Lymphoma. Pineoblastoma. Neuroblastoma. Medulloblastom. Metastases: Melanoma. Lung carcinoma. Colon carcinoma. Breast carcinoma.
Some specialized areas of the brain have no blood-brain barrier and will normally enhance
Choroid plexus. Pituitary glands. Pineal glands. Tuber cinereum. Area postrema.
Tumor enhancement generally means
Aggressive, high-grade neoplasms tend to have fenestrated capillaries (blood-brain barrier breakdown) allowing for enhancement.
Postop granulation tumor versus residual tumor?
Granulation tissue generally forms 72 hours after surgery. Early (less than 72 hours) postop enhancement likely reflects residual tumor rather than granulation tumor.
Diffuse white matter radiation injury
Unenhancing geographic white matter T2 hyperintensity conforming to radiation ports. Develops 6 months postradiation therapy.
Indistinguishable from recurrent tumor on conventional imaging. May demonstrate mass effect and enhancement. Radiation necrosis may have elevated lactate peak (necrosis) on MRS. Recurrent tumor may have elevated choline peak and depressed n-acetyl aspartate (NAA) peak.
Astrocytoma grades and types
Grade I (pilocytic astrocytoma, subependymal giant cell astrocytoma). Grade II (lack necrosis and endothelial proliferation). Grade III (anaplastic astrocytoma). Grade IV (necrosis and endothelial proliferation, Glioblastoma multiforme).
Female predominant brain tumors
Meningioma (4:1). Neurofibroma. Pineocytoma. Pituitary tumor.
Male predominant brain tumors
Pineal germinoma (10:1). Pineal parenchymal tumor (4-7:1). Medulloblastoma (3:1). Glioblastoma multiforme (3:2). Choroid plexus papilloma (2:1). CNS lymphoma. Hamartoma of tuber cinereum.
Two neoplasms that may exhibit bihemispheric spread through the corpus callosum.
Glioblastoma multiforme. CNS lymphoma.
Intra-axial Lesions With Marked Surrounding Edema
Metastases. Abscess. Glioblastoma multiforme. Radiation necrosis. Hematoma (mild).
Hemorrhagic Brain Tumors
Primary: Glioblastoma multiforme (most common overall). Oligodendroglioma. Metastasis: RCC. Thyroid carcinoma. Choriocarcinoma. Melanoma.
Cerebral Ring-Enhancing Lesions
MAGIC DR. Metastasis. Abscess. Glioblastoma multiforme. Infarct. Contusion. Demyelinating disease. Resolving hematoma. radiation necrosis.
This MR sequence may help distinguish acute infarct from low-grade neoplasm.
DWI. Infarct exhibitis restricted diffusion.
Rare neoplastic infiltration of at least three lobes of the brain. Poor prognosis. Diffuse involvement of cerebral white matter with or without a mass.
In an adult with a heterogeneous calcified mass within the periphery of a frontal lobe with calvarial erosion and relative absence of edema should suggest the diagnosis of
Grade II tumor. Commonly located in the frontal lobes. Often extends to cortex and may erode calvarium. 70% calcify.
Calcified Glial Tumors in Order of Frequency
Old Elephants Age Gracefully: Oligodendroglioma. Ependymoma. Astrocytoma. Glioblastoma multiforme.
CNS lymphoma imaging characteristics
Hyperdense and T1 hypointensity on T2WIs with surrounding vasogenic edema. Subependymal spread is common. Bihemispheric involvement via corpus callosum may be seen.
Ganglioglioma and Gangliocytoma
Ganglioglioma contains glial cells and differentiated neurons. Most common tumor seen with chronic temporal lobe epilepsy. Gangliocytoma and ganglioneuroma are pure neuronal tumors without glial components. Floor of third ventricle is the most common location for gangliocytoma.
Desmoplastic Infantile Ganglioglioma
Rare variant of ganglioglioma seen in the first year of life. Very large heterogeneous mass with intense enhancement.
Most common tumor associated with medically refractory partial complex seizures
Dysembryoplastic neuroepithelial tumor. Always involves cortical gray matter. May have “soap bubble” appearance with exophytic extension beyond cortical gray matter margin.
Congenital Brain Tumors in Infants Younger Than 60 Days Old
Teratoma (most common): Two thirds are supratentorial. Primitive neuroectodermal tumors: Curvilinear, sparse calcification. Astrocytoma. Choroid plexus papilloma. Ependymoma. Medulloepithelioma. Germinoma. Angioblastic meningioma. Ganglioglioma.
Most (80% to 85%) metastatic lesions occur supratentorially, with the exception of ___________, which has a predilection for the posterior fossa.
Renal cell carcinoma.
Most Common Intra-axial Metastases to the CNS
Lung. Breast. Melanoma. Colon cancer.
Most Common Extra-axial Metastases to the CNS
Breast. Prostate. Lung. Neuroblastoma.
Most Common Hemorrhagic Metastases to the CNS
Melanoma. Renal. Thyroid. Choriocarcinoma.
Malignant invasion of leptomeninges. May mimic meningitis. Commonly involves basal cisterns. May present with cranial nerve palsies. Common malignancies: Breast. Lung. Lymphoma. Leukemia. Primary CNS malignancies.
Most common primary cerebellar neoplasm in adult population.
Most reliable way to differentiate a medulloblastoma from an astrocytoma on cross-sectional imaging studies is
Noncontrast CT scan. Astrocytoma will usually be hypodense. Medulloblastoma will almost never be hypodense.
Posterior Fossa Masses in Children: Medulloblastoma
Most common pediatric CNS malignancy. Majority (85%) arise from cerebellar vermis. Commonly extends into fourth ventricle causing hydrocephalus. Highly malignant neoplasm (WHO grade IV). Hyperdense on CT. Hypointense on T1WIs. Variable on T2WIs.
Posterior Fossa Masses in Children: Pilocytic astrocytoma
Location: Cerebellar vermis. Hemisphere. Cystic with enhancing nodule.
Posterior Fossa Masses in Children: Ependymoma
Location: 4th ventricle. Appearance: Foraminal extension. Heterogeneous on CT and MR. Intense but heterogeneous enhancement.
Posterior Fossa Masses in Children: Brainstem glioma
Location: Brainstem. Appearance: Expansile brainstem. Isodense to hypodense on CT. Hypointense on T1WIs. Hyperintense on T2WIs.
Most common brain tumor seen in neurofibromatosis type 1 (NF1)
Cystic cerebellar mass with an enhancing mural nodule suggests two possible diagnoses, and the best discriminator between the two is
Age. Pilocytic astrocytoma, peak age of birth to 9 years. Hemangioblastoma, peak age of 35 years.
Benign neoplasms of endothelial origin. Most common primary cerebellar neoplasm in adults. 4% to 20% occur as part of von Hippel-Lindau syndrome. Occur most often in cerebellar hemispheres and spinal cord. Well-defined cystic mass with an intensely enhancing mural nodule.
Dysplastic Cerebellar Gangliocytoma (Lhermitte-Duclos Disease)
Likely a hamartoma. Half of patients have Cowden disease (phacomatosis, colonic polyps, cutaneous tumors, meningioma, glioma, thyroid, breast neoplasms). CT often is normal. Striated cerebellar mass on T1and T2 WIs.
Most common extra-axial neoplasm of adults. Peak age of 50 to 60 years. Occur more commonly within women. Multiple tumors are associated with neurofibromatosis. Common locations: Parasagittal or convexity locations (50%). Sphenoid wing (20%). Olfactory groove/planum sphenoidale (10%). Parasellar region (10%). Hyerdense, hyperenhancing mass with variable surrounding edema. Calcification occurs in 10% to 20% of cases. Angiographically, early dense tumor blush that persists well into venous phase,
Cerebral Intraventricular Masses
Choroid plexus papilloma (24%). Choroid plexus carcinoma (2%). Ependymoma (18%). Subependymoma (11%). Central neurocytoma (10%). Subependymal giant cell astrocytoma (6%). All other astrocytomas (9%). Meningioma (6%). Colloid cyst (4%). Metastasis (2%).
Most Common Lateral Ventricle Masses, by Location and Age: 0 - 10 yo, Ventricle Body
PNET (Primitive neuroectodermal tumor). Teratoma. Choroid plexus papilloma.
Most Common Lateral Ventricle Masses, by Location and Age: 0 - 40 yo, Ventricle Trigone
Choroid plexus papilloma.
Most Common Lateral Ventricle Masses, by Location and Age: 10 - 40 yo, Foramen of Monro
Subependymal giant cell astrocytoma. Pilocytic astrocytoma.
Most Common Lateral Ventricle Masses, by Location and Age: 10 - 40 yo, Ventricle Body
Ependymoma. Pilocytic astrocytoma. Central neurocytoma.
Most Common Lateral Ventricle Masses, by Location and Age: > 40 yo, Ventricle Body
Most Common Lateral Ventricle Masses, by Location and Age: > 40 yo, Ventricle Trigone
Choroid Plexus Papilloma
Most commonly occurs in lateral ventricle, especially in children. Increased intracranial pressure and hydrocephalus due to: Increased tumor production of CSF. Impaired CSF resorption (tumoral hemorrhage). CSF obstruction (mass effect). WHO grade I. May engulf glomus of choroid plexus. Choroid plexus calcification in first decade of life suggests choroid plexus papilloma.
Arises from septum pellucidum or ventricular wall. 50% occur in lateral ventricle near foramen of Monro. May be bilateral. Most patients (75%) are between 20 and 40 years. Well-circumscribed lobulated mass within lateral or third ventricles. Hyperdense at CT. Cystic elements (Swiss cheese) and calcification are common.
WHO grade I. Most are asymptomatic. Well-circumscribed lobulated intraventricular mass. Isodense to hypodense at CT. Frequent calcification (33%) and cystic degeneration (20%). Low T1 and high T2 signal. Hypointensity on T1WIs and hyperintensity on T2WIs are seen on MR. Enhancement not as diffuse as in central neurocytoma.
Subependymal giant cell astrocytoma
Seen in 10% of patients with tuberous sclerosis (look for subependymal and cortical hamartomas). WHO grade I. Commonly calcifies. and slow-growing, with calcification a common feature. Almost always produces some degree of hydrocephalus.
Occurs in anterosuperior portion of third ventricle near foramen of Monro. Can cause acute hydrocephalus. Almost all are hyperdense. Variable T1 and T2 signal.
Masses of the Anterosuperior Third Ventricle
Colloid cyst. Meningioma. Choroid plexus papilloma. Hamartoma. Glioma. Vascular lesion. Granulomatous disease.
Most common neoplasm of pineal region
Germ cell tumors
Calcified pineal mass in a female is more likely to be
Pineocytoma. In a male more likely to be a germinoma.
When calcification in the pineal region exceeds ____ in size, a pathologic pineal process should be suspected.
Cerebral Germ cell tumors
Well-defined, usually midline masses. 65% occur in pineal region (male more than female). 60% of all pineal masses. 35% are suprasellar (male = female). Germinoma is by far the most common. Commonly seen in children and young adults.
Pineal region masses
Germ Cell Tumors (60%): Germinoma. Teratoma. Embryonal carcinoma. Endodermal sinus tumor. Choriocarcinoma. Pineal Parenchymal Tumors (14%): Pineocytoma. Pineoblastoma. Other: Pineal cyst, glioma, tentorial meningioma, vein of galen malformation, arachnoid cyst, lipoma.
Similar to medulloblastoma, part of PNET spectrum. Majority occur in young children. Well-circumscribed, often lobular. Local invasion and frequent calcification. WHO grade IV. Rarely may occur with bilateral retinoblastomas, the so-called trilateral retinoblastoma.
Most commonly seen in adults (women more than men). Usually well demarcated, noninvasive, and slow growing. Often calcified. Rarely metastasizes. At imaging, can't be differentiated from pineal germinoma or pineoblastoma.
Are common. Signal similar to or slightly higher than CSF, likely due to lack of CSF puslation. No enhancement.
Most common sellar masses. Microadenomas (10 mm or smaller). Macroadenomas (>10 mm). 75% are hormonally active, most of which are microadenomas. Lateral gland generally contains prolactin and growth hormone secreting adenomas. Central gland generally contains ACTH, TSH, FSH secreting adenomas. Microadenomas best detected on coronal T1WIs: Focal hypointensity (on noncontrast studies).
Arise from squamous epithelial remnants of anterior lobe of pituitary gland. Commonly are symptomatic due to large size. Most common suprasellar mass in children. Peak incidence between 5 and 10 years of age and 50 and 60 years. Solid and cystic components are typical. Large cystlike sellar/suprasellar mass with enhancing rim and some calcification. T1 (liquid crystal) and T2 hyperintense cyst.
Rathke cleft cyst
Arise from squamous epithelial remnants of anterior lobe of pituitary gland. Usually asymptomatic. Cyst may contain mucus, serous fluid, or cellular debris. Variable signal intensities. May mimic craniopharyngioma.
Arises from Schwann cells. Commonly affects vestibulocochlear (VIII) and trigeminal (V) nerves. Cystic degeneration is common, especially in larger lesions. T1 hypointense to gray matter and T2 hyperintense to gray matter. Intense enhancement.
Most helpful imaging feature in distinguishing vestibular schwannomas
Extension of enhancement along course of seventh and eighth nerves.
SATCHMO Sella (pituitary) tumor. Sarcoid. Aneurysm. Arachnoid cyst. Teratoma. Craniopharyngioma. Hypothalamic glioma. Hamartoma of tuber cinereum. Histiocytosis. Meningioma. Optic nerve glioma.
AMEN Acoustic (vestibular) schwannoma. Meningioma. Ependymoma. Neuroepithelial cyst (arachnoid, epidermoid).
Epidermoid versus Dermoid
Epidermoid: Common. 40 to 50 yo. Ectoderm. Off midline (cerebellopontine cistern, parasellar, posterior fossa). Follows CSF, except hyperintense on DWI. Lobulated with peripheral enhancement. Dermoid: Uncommon. 20 to 30 yo. Ectoderm and mesoderm. Midline (pericerebellar, suprasellar). Typical fat attenuation or signal.
Occur within all age groups. Most common locations: Interhemispheric falx (often associated with agenesis of corpus callosum). Quadrigeminal plate. Suprasellar regions. Chemical shift artifact or fat suppression. Presence of flow void or traversing cranial nerve favors lipoma and excludes dermoid.
Are intra-arachnoidal. 50% occur in middle cranial fossa. Other sites: Frontal convexity. Suprasellar and quadrigeminal cisterns. Posterior fossa. Follow CSF signal and density. May remodel adjacent bone. Do not restrict diffusion. Enlarged cisterna magna fills immediately at cisternography; whereas, arachnoid cyst may not fill or slowly fill.
Hamartoma of tuber cinereum
Rare congenital hamartoma. More common in boys. Precocious puberty, gelastic seizures, developmental delay, and hyperactivity. Well-circumscribed, round or oval mass centered at the tuber cinereum (base of infundibulum). Does not calcify or hemorrhage. Stalk connecting mass with tuber cinereum or mamillary bodies cinches diagnosis.
Granuloma with central caseous necrosis. Isodense or slightly hyperdense nodules or small mass lesions.
Occurs in southwestern United States. Focal parenchymal granulomas are rare. Hydrocephalus is common from complicating meningitis.
Occurs in Ohio and Mississippi River valleys. Frequently presents with meningitis with parenchymal abscesses and granulomas less likely. Epidural granulomas and abscesses also occur usually from direct extension from bone infection.
Occurs in Midwest and southern United States. Meningitis is most common. Multiple or solitary granulomas may occur.
Parenchymal disease usually takes the form of an abscess. Granulomas are unusual. Abscesses are often multiple with irregular ring enhancement. Subcortical or cortical infarcts and hemorrhage from blood vessel invasion may occur.
Invades brain usually by direct extension from sinuses, nose, or oral cavity. Almost all patients are diabetic or immunocompromised. Tends to invade blood vessels. Lesions are often in the base of the brain, adjacent to diseased sinuses. Infarcts, intra-axial or extra-axial hemorrhage, and meningeal enhancement can be seen with CT or MR.
Usually causes meningitis. Granulomas and small abscesses may occur. Meningeal enhancement or multiple small enhancing granulomas or microabscesses are usually seen.
Most frequently reported CNS fungal infection.
50% occur in immunocompetent patients. Common infection in patients with AIDS. Usually presents as meningitis. Granulomas can occur and are usually multiple. Abscesses are less common. CT scans can be normal. Cryptococcomas are small, usually multiple, solid-enhancing, peripheral parenchymal nodules. Gelatinous pseudocysts can be seen.
Cystic lesion usually in basal ganglia. Perivascular spaces filled with cryptococcal organisms. Usually found only in immunocompromised.
Caused by larvae of pork tapeworm Taenia solium. Ingested eggs hatch in intestine and larvae are hematogenously distributed, forming cysticerci. 3 stages of CNS disease: Early phase, edema and/or nodular enhancement. Later, peripheral viable cysts. Scolex may be seen as small mural nodule. Late phase, peripheral calcifications without edema or enhancement.
Caused by dog tapeworm. More commonly involves liver and lungs, but brain can rarely be involved. Cysts are usually solitary, unilocular, large, round, and smoothly marginated. Most often supratentorial, in the middle cerebral artery territory.
Congenital CNS toxoplasmosis
Atrophy, dilated ventricles, and calcifications. Periventricular white matter, basal ganglia and cerebral hemisphere calcifications. In CMV, calcifications are usually periventricular only.
Amebae enter nasal cavity of patients swimming in infested water. Direct extension through cribriform plate to the brain. Severe meningoencephalitis results and is usually fatal. Early in infection, meninges and gray matter may enhance. Later, diffuse cerebral edema ensues.
Symptomatic patients may have aseptic meningitis, tabes dorsalis, general paresis, or meningovascular disease. Imaging is usually normal in tabes dorsalis, rarely gummas are found: small enhancing nodules on brain surface with adjacent meningeal enhancement. Meningovascular syphilis thickening of meninges and medium to large vessel arteritis.
CNS Lyme disease
2 Forms. Cranial neuritis: Thick, enhancing nerves. CNs III to VIII may be involved (CN VII most common). Parenchymal form: Multiple small white matter lesions. Similar to multiple sclerosis. Lesions may have nodular or ring enhancement. Meninges may enhance.
Cytomegalovirus, congenital CNS infection
Most common CT findings: Periventricular calcification. No calcifications of basal ganglia or cortices as seen congenital toxoplasmosis.
Neonatal herpes simplex encephalitis
Early in course: Diffuse brain swelling or bilateral patchy areas of decreased density (hypoechoic, too) in cerebral white matter and cortex. Sparing of basal ganglia, thalami, and posterior fossa structures. Multicystic encephalomalacia is the end result.
Adult herpes simplex CNS infection
May cause encephalitis or cranial neuritis. 70% mortality rate in untreated patients. Ill-defined hypodensities within one or both temporal lobes. Virus is usually latent within gasserian ganglion. Frontal lobes may be involved. Insular cortex is often involved, but adjacent putamen is spared. Usually swelling with mass effect. Streaky enhancement is variable. The CT findings are not usually seen before the fifth day of symptoms. Increased FLAIR and T2 signal within temporal and/or frontal lobe(s) with sparing of putamen. Middle cerebral artery infarct (often involves putamen, unlike herpes).
Ramsay Hunt syndrome
Herpes zoster facial neuritis. Ear pain, facial paralysis, vesicular eruption about the ear. MR may reveal increased enhancement of facial nerve.
Acute disseminated encephalomyelitis (ADEM)
May occur after viral infection, following a vaccination, or spontaneously. When treated early with steroids, most patients make a full recovery. Increased T2 and FLAIR signal within white matter of brainstem, cerebellum, and basal ganglia. Optic neuritis is also common.
Subacute sclerosing panencephalitis
caused by variant of measles virus. Occurs in children and young adults who had measles before age 2, after a 6- to 10-year asymptomatic period. Causes progressive dementia, seizures, and paralysis, leading to death. Initially may have focal lesions in gray matter and subcortical white matter. Later, periventricular white matter lesions may enhance. Late stages usually is profound cortical atrophy.
Progressive multifocal leukoencephalopathy (PML)
Demyelinating disease caused by a papova virus. Occurs only in immunosuppressed patients, especially in AIDS.
Caused by a prion. Rapidly progressive dementia, ataxia, and myoclonus, leading to death. Early stage, high DWI signal within cerebral cortex and basal ganglia. Later stage, atrophy and increased T2 and FLAIR signal within cortex and basal ganglia.
Meningitis forms causing thick meningeal enhancement (pachymeningeal)
Tuberculous meningitis. Fungal meningitis. Racemose cysticercosis. Sarcoidosis.
Most common AIDS CNS infections
HIV encephalopathy. Toxoplasmosis. Cryptococcosis. Other fungal infections. CMV and Herpes meningoencephalitis. Mycobacterial infection. PML. Meningovascular syphilis.
Most common CNS AIDS tumor
Primary CNS lymphoma.
Diffuse atrophy is most common manifestation. White matter lesions are seen with AIDS dementia complex. Diffuse pattern of increased T2 signal in deep white matter or multiple small punctate white matter lesions.
Most common opportunistic CNS infection in AIDS
Multiple high T2 signal and enhancing mass lesions (1-4 cm) with surrounding vasogenic edema. Larger lesions usually exhibit ring enhancement. Unlike bacterial abscesses, toxoplasmosis lesions are not high in signal on DWI. Preferred sites: Basal ganglia. White matter. Cortex. Main differential consideration is primary CNS lymphoma.
Most common AIDS CNS fungal infection
Progressive multifocal leukoencephalopathy
Infection of immunosuppressed patients (AIDS, transplants, leukemics) caused by reactivation of JC virus. Progressive course to death within months. In non-AIDS patients, has a predilection for occipital lobes. In AIDS patients, any part of brain may be involved. High T2 and low T1 lesions within subcortical and deep white matter. Mass effect and contrast enhancement are almost always absent.
Primary CNS lymphoma
Most common intracranial tumor in AIDS. Solitary or multiple enhancing mass lesions, centrally located within deep white matter or basal ganglia. Lesions usually are T2 isointense to white matter with homogeneous enhancement. Toxoplasmosis lesions usually are T2 hypointense.
Inherited disorder (leukodystrophy), affecting formation or maintenance of myelin. Generally encountered within pediatric population.
Acquired disorder that affects normal myelin. Generally encountered within adult population.
Multiple sclerosis (MS, Primary Demyelination)
Multiple CNS lesions separated in time and space. Typical lesions are high T2 signal and round or ovoid in a periventricular (perpendicular to ventricle) or subcortical location. Enhancement reflects new lesions. Dark T1 lesions are due to acutal neuronal tissue loss. Other sites affected: Cerebellar and cerebral peduncles. Corpus callosum. Medulla. Spinal cord. Conglomerate large lesions may be mistake for a neoplasm (tumefactive).
Involvement of callosal-septal interface is quite specific for
Nonspecific punctuate white matter lesions (small bright lesions on T2WIs) are more prominent in any patient with
Vasculopathy or hypercoagulable state.
A classic case presentation is that of a young adult female with prior miscarriages presenting with headaches/migraines and ischemic white matter changes.
Antiphospholipid syndrome (phospholipid antibody syndrome). Hypercoagulable state with white matter and ischemic changes.
Normal anatomic finding. May mimic pathology. High T2 signal at tips of frontal horns. Due to porous ependyma allowing transependymal flow of CSF.
Senescent periventricular hyperintensity
Age-related high T2 signal along entire length of lateral ventricles.
Prominent perivascular spaces
CSF-filled perivascular clefts. Also called Virchow-Robin spaces. Punctate foci of high T2 signal. Typically within centrum semiovale and lower basal ganglia at the level of the anterior commissure, where lenticulostriate arteries enter the brain.
MR sequences that help distinguish perivascular spaces from parenchymal lesions
Proton-density and FLAIR sequences. PD: CSF has similar signal intensity as white matter. Perivascular space is isointense to brain. Ischemic lesions are bright due to gliosis. FLAIR: Parenchymal lesions with gliosis have abnormal signal.
Central pontine myelinolysis (CPM)
Demyelination of central pons. Due to electrolyte abnormalities, particularly hyponatremia, that are rapidly corrected. Oligodendroglial cells are most susceptible: Central pons. Thalamus. Globus pallidus. Putamen. Lateral geniculate body.
Posterior reversible encephalopathy syndrome (PRE)
Symmetric subcortical and cortical vasogenic edema within parietooccipital lobes. Temporary failure of autoregulation of cerebral arteries. Associations: Cyclosporin A or tacrolimus (FK506). Acute renal failure/uremia. Hemolytic uremic syndrome. Eclampsia. Thrombotic thrombocytopenia purpura. Chemotherapy (interferon).
Rare demyelination seen frequently in alcoholics. Involves central fibers (medial zone) of corpus callosum. Anterior and posterior commissures. Centrum semiovale. Mddle cerebral peduncles. Felt to reflect a form of osmotic demyelination
Wernicke encephalopathy and Korsakoff syndrome
Metabolic disorders caused by thiamine (B1 vitamin) deficiency: alcoholics, hematologic malignancies, hyperemesis gravidarum. Wernicke encephalopathy clinical triad of acute ocular movement abnormalities, ataxia, and confusion. If longterm memory and learning problems result then Korsakoff syndrome. Early stage may reveal T2 hyperintensity or contrast enhancement of mamillary bodies, basal ganglia, thalamus, brainstem, and periaqueductal involvement. Chronic stage may show mamillary body and tegmentum atrophy and dilation of third ventricle.
Occurs 6 to 9 months after treatment in excess of 40 Gy. Confluent high T2 signal within white matter extending to subcortical U fibers.
Commonly occurs 6 to 24 months postradiation. Enhancing lesion with mass effect and ring enhancement. Or multiple foci of enhancement, Mimicks recurrent neoplasm. MR spectroscopy (MRS): Elevated lactate and lipids (0.9 to 1.3 ppm). Reduced other major metabolites (choline, creatine, and N-acetylaspartate).
Metachromatic leukodystrophy: head size, age of onset, white matter involvement, gray matter involvement
Normal head size. Infantile form 1-2 yo. Juvenile form 5-7 yo. Diffuse white matter involvement. No gray matter invovlement. Most common Leukodystrophy. Deficiency of the enzyme arylsulfatase A.
Adrenoleukodystrophy leukodystrophy: head size, age of onset, white matter involvement, gray matter involvement
Normal head size. 5-10 yo. Symmetric occiptal and splenium of corpus callossom white matter invovlement. No gray matter involvement. Sex-linked recessive condition (peroxisomal enzyme deficiency) occurring only in boys.
Leigh disease: head size, age of onset, white matter involvement, gray matter involvement
Normal head size. Less than 5 yo. Focal areas of subcortical white matter. Basal ganglia and periaquaductal gray matter involvement. Also called subacute necrotizing encephalomyelopathy. Mitochondrial enzyme defect.
Alexander disease: head size, age of onset, white matter involvement, gray matter involvement
Normal to large head size. Less than 1 yo. Frontal white matter involvement. No gray matter involvement.
Canavan disease: head size, age of onset, white matter involvement, gray matter involvement
Normal to large head size. less than 1 yo. Diffuse white matter involvement. Vacuolization of cortical gray matter. deficiency of aspartoacylase, leads to the buildup of NAA (MRS).
Transependymal flow of CSF
Occurs in acute hydrocephalus. May mimic periventricular white matter disease. Important means of CSF reabsorption during ventricular obstruction.
CSF circulation route
Produced mainly by choroid plexus of lateral, third, and fourth ventricles. Flows from lateral ventricles through foramina of Monro to third ventricle through cerebral aqueduct to fourth ventricle through lateral and medial fourth foramina (Luschka and Magendie) to basilar cisterns and over hemisphere surfaces. Principal site of absorption is into venous circulation through arachnoid villi.
Will commonly demonstrate supratentorial ventriculomegaly, with a fourth ventricle that appears normal.
Communicating hydrocephalus. Dilated 4th ventricle can be seen in communicating and non-communicating hydrocephalus.
Ex Vacuo Ventriculomegaly
Enlarged ventricles due to cerebral atrophy. Prominence of both sulci and ventricles.
Normal pressure hydrocephalus
Chronic, low-level form of hydrocephalus. Clinical triad: Dementia, gait disturbance, and urinary incontinence. CSF pressure is within normal limits. Slight gradient exists between ventricular system and subarachnoid space due to incomplete subarachnoid CSF block. Commonly results from prior subarachnoid hemorrhage or meningitis. Diffuse ventriculomegaly out of proportion to sulcal prominence. Early entry of radiotracer into lateral ventricles, with persistence at 24 and 48 hours. Delay ascent to parasagittal region.
Alzheimer disease (AD)
Most common cause of dementia. Prefential atrophy of: Hippocampal formation. Temporal lobes. Parietotemporal cortices. Enlargement of temporal horns, suprasellar cisterns, and sylvian fissures may distinguish from age-related atrophy.
Most common basal ganglia disorder. Deficiency of dopamine specifically within pars compacta of the substantia nigra. MR imaging is relatively insensitive but is useful in excluded other causes of movement disorders (stroke).
Progressive hereditary disorder occuring in fourth and fifth decades. Findings: Diffuse cortical atrophy. Caudate nucleus atrophy. Putamen atrophy. Enlargement of frontal horns (heart-shaped).
Hepatolenticular degeneration. Inborn error of copper metabolism. Hepatic cirrhosis and degenerative changes of basal ganglia. Diffuse atrophy with signal abnormalities involving deep gray matter nuclei and deep white matter.
Bilateral lesions of basal ganglia can be seen in a variety of insults
Carbon monoxide exposure (globus pallidus). Methanol toxicity (putaminal). Metabolic conditions (Wilson disease). Hallervorden-Spatz disease (iron deposition within globus pallidus). Mitochondrial disorders (Leigh disease and Kearns-Sayre syndrome).
Myelination Landmarks by Age 0 days
High T1 signal: Dorsal brainstem. Ventrolateral thalamus. Lentiform nucleus. Central corticospinal tracts. Low T2 signal: Posterior limb internal capsule posterior portion.
Myelination Landmarks by Age 3 months
High T1 signal: Anterior limb internal capsule. Cerebellar white matter.
Myelination Landmarks by Age 6 months
High T1 signal: Genu of corpus callosum. Low T2 signal: Splenium of corpus callosum.
Myelination Landmarks by Age 11 months
Low T2 signal: Anterior limb internal capsule.
Myelination Landmarks by Age 18 months
Adult appearance except for terminal myelination zones (periatrial and adjacent to frontal horns)
Myelination Landmarks by Age 24 months
Dark white matter on T2 (some minimal high-signal areas may persist peripherally)
Rare X-linked leukodystrophy. Arrest of myelin development, usually in neonatal period. Shows lack only of myelin formation, rather than myelin formation followed by destruction.
HYPOXIC ISCHEMIC ENCEPHALOPATHY (HIE)
Damage to brain from hypoxia/ischemia occurring in utero or around time of delivery.
Ischemic infarction of both cerebral hemispheres. Early compromise of both carotid arteries with preservation of posterior circulation. Mimics severe hydrocephalus (thin rind of cortical gray matter). Complete infarction of supratentorial cerebral tissues with preservation of thalami and cerebellum.
Hypoxic ischemic encephalopathy occuring within 1st trimester
Cortical irregularity and/or hydranencephaly.
Hypoxic ischemic encephalopathy occuring at less than 26 weeks of gestation
Periatrial injury. No gliosis. Ex vacuo enlargement.
Hypoxic ischemic encephalopathy occuring at greather than 28 weeks
Periatrial gliosis: high T2 signal.
Hypoxic ischemic encephalopathy occuring at term
Watershed infarcts. Ulegyria. Variable deep, superficial white matter gliosis and atrophy. Myelination delay. Injury to hippocampus and pons.
Periventricular Leukomalacia (PVL)
Occurs in term infants, premature infants greater than 26 weeks of gestation. Periventricular gliosis. Ex vacuo ventriculomegaly. Apposition of sulci to ventricular surface.
Gliosis in the periatrial region (seen best on proton-density scans) is caused by injury to the developing brain at ______ gestational age or older.
28 weeks .
Ex vacuo atrial enlargement without gliosis reflects injury prior to _______ gestational age.
Acute imaging findings of Profound Perinatal Hypoxic Ischemic Injury
Deep gray matter: Isodense to white matter. Mottled high T1 and low T1 signal. White matter: Normal. May see blurred gray-white junction on protein density images.
Subacute imaging findings of Profound Perinatal Hypoxic Ischemic Injury
Deep gray matter: Variable T1 and T2 signal. White matter: High T1 and low T2 perirolandic cortex.
Chronic imaging findings of Profound Perinatal Hypoxic Ischemic Injury
Deep gray matter: High T2 signal. White matter: High T2 perirolandic cortex. Thinned gyri, atrophy.
Imaging of Profound Postnatal Hypoxic Ischemic Injury
Deep gray (Damage to corpus striatum: high signal on T2WIs Relative sparing of thalami) Cortex (Majority of cortex injured: high signal on T2WIs Relative sparing of perirolandic cortex Thinned gyri)
Septo-optic dysplasia (SOD)
Congenital disorder with variable hypoplasia of optic nerves and complete or partial absence of septum pellucidum. Squared-off appearance of frontal horns.
Poor prognosis. Anterior rind of brain tissue and monoventricle communicating with dorsal cyst. Fused thalami. Absent septum pellucidum, corpus callosum, and falx. Upside-down U-shaped mantle of brain tissue. Ends of U are hippocampal ridges.
Partial fusion of hemispheres. Absent or dysgenic corpus callosum and septum pellucidum. High association with migration anomalies. Posterior portion of interhemispheric fissure and falx are usually formed.
Partial absence of frontal interhemispheric fissure. Absent septum pellucidum and relatively normal brain overlap with SOD. Body and splenium of corpus callosum are usually present with genu and rostrum absent (dysgenic corpus callosum).
Lipomas of corpus callosum
Congenital abnormalities. High T1 signal with fat supression. No mass effect. Vessels course through these lesions. Occur because of persistence of meninx primitiva.
Lissencephaly and pachygria/agyria complex
Synonyms meaning absence of gyri. Smooth hourglass brain. Thick, multilayered cortex. Classic pattern: Arrested neuronal migration with only four cortical layers. Premature infant's brain can be a mimic.
Asymmetric hemispheric enlarged with polymicrogyric and pachygyric changes. May be associated with neurofibromatosis.
Polymicrogyria and pachygria
Pachygyria is a incomplete lissencephaly. Broad, thick gyri with shallow sulci. Normal interdigitating fingers of subcortical white matter are absent. Polymicrogyria is a cortical dysplasia. Thick mantle of gray matter with multiple small gyri. Normal interdigitating fingers of subcortical white matter are absent. Underlying white matter gliosis in polymicrogyria can sometimes help differentiate it from pachygyria.
Heterotopic Gray Matter
Islands of gray matter anywhere between ependymal surface and subcortical white matter. May cause seizures.
Abnormal neuronal migration resulting in gray matter-lined clefts that invaginate brain. Extend from ventricular ependymal surface to pial cortical surface. Polymicrogyric clefts do not extend to ventricle. Open lip or closed lip (apposed walls) forms.
Distinguishing porencephaly from open lipped schizencephaly
Porencephaly: encephalomalacia that communicates with ventricle. Schizencephalic clefts are lined by gray matter. Porencephalic cysts are lined by a thin layer of white matter.
Chiari II malformations
Small posterior fossa: Cerebellum is squeezed up against tentorium, down through foramen magnum (tonsillar herniation), and forward around brainstem. Pons and medulla are squeezed inferiorly with cervicomedullary kink. Cord syrinx is present. Nearly all have hydrocephalus. Most have partial or complete agenesis of corpus callosum. Most present with myelomeningocele.
Chiari I malformations
Cerebellar tonsillar ectopia (tonsils extend > 5 mm below foramen magnum). Patients may be asymptomatic. May give rise to cervical spinal cord syrinx.
Large posterior fossa with high tentorial insertion. Dilated cystic 4th ventricle fills posterior fossa. Cerebellar vermis and hemispheres may be hypoplastic or absent.
Neurofibromatosis type 1 imaging findings (chromosome 17)
Altered signal in white matter and basal ganglia. Dural ectasia. Optic and other gliomas. Sphenoid dysplasia. Thinning long bone cortex (ribbon ribs). Plexiform neurofibromas. Café au lait spots. Iris hamartomas (Lisch nodules). Vascular stenoses.
Neurofibromatosis type 2 imaging findings (chromosome 22)
Vestibular schwannomas. Meningiomas. Spinal glial tumors. Optic and other gliomas.
Skin lesions: Adenoma sebaceum. Ash-leaf spots. Brain lesions: Subependymal hamartomas. Cortical tubers. Subependymal giant cell astrocytomas located at foramina of Monro (May lead to hydrocephalus)
Skin and meningeal angiomatous lesions. Port-wine nevus: skin angioma in ophthalmic division of trigeminal nerve. Pial angiomas may result in chronic ischemia, gliosis, and gyral cortical calcifications. Enlargement of deep and subependymal veins may mimic arteriovenous malformations.